NBME 21 Answers ↦
A helpful equation is CO=rate of O2 consumption/(arterial O2 content-venous O2 content): Fick principle
If CO is decreased, then the difference between arterial O2 content and venous O2 content is increased
To clarify a little bit, the tissues wouldn't necessarily extract MORE oxygen from the passing RBCs than they normally would. They would extract the same amount as they normally would to carry out their own functions. However, because the starting amount of O2 delivered to tissues is lower, you'd end up with less O2 bound to hemoglobin returning to the right heart.
no, decreased CO => peripheral vasoconstriction => SVR will be increased
No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs )
Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI?
@snafull: my initial thought is that we would see pulmonary vasoconstriction because of the relatively low oxygen tension (that results from the low cardiac output).
crackles are heard bilaterally so there is pulm patho which leads to increased pulm vascular resistance, since systemic blood flows into the lungs.
any block in the flow ahead (lungs) will increase resistance in flow behind ( systemic )
This patient is hypoxic increased diffusion distance. This causes pulmonary vasoconstriction. Ordinarily this response is designed to shunt blood to parts of the lungs that are well ventilated, but the response is maladaptive in global hypoxia
I dont believe decreased venous oxygen tension would lead to pulmonary vasoconstriction (this is typically in the setting of low PAO2 you see this; shunting blood away from poorly oxygenated alveoli). You can get to increased pulmonary vascular resistance due to pulm edema from Left heart failing leading to fluid overload in pulm vasculature).